Role of Histamine in Hypoxic Pulmonary Hypertension in the Rat

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Abstract
Pharmacological agents that block or potentiate the effects of naturally occurring vasoactive substances were used to try to determine which substance, if any, mediates the vasoconstrictor response to acute alveolar hypoxia in isolated rat lungs. Isolated and ventilated lungs of rats were perfused at 37°C with homologous blood at constant-volume, pulsatile inflow, and pressor responses to brief periods of ventilation hypoxia (2% O2) were recorded (control, 21% O2). Antihistamines of four different chemical classes in concentrations of 70 to 140 µg/ml abolished all pressor responses to alveolar hypoxia without interfering with the effects of injected bradykinin, ATP, or serotonin. A histaminase-inhibiting compound, semicarbazide, potentiated the hypoxic pressor response. The hypoxic pressor response could not be abolished by α-receptor-, serotonin-, or ATP-blocking agents. The results suggest that endogenous histamine in the lung is involved in the vasoconstrictor response to acute alveolar hypoxia.

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